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16 Cards in this Set
- Front
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List the 5 main toxic plants |
1) Ragwort 2) Yew 3) Cardiac glycoside-containing plants 4) Oak (acorn poisoning) 5) Selenium toxicity |
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Yew Toxicity 1) What is the toxic component? 2) How does it work? 3) What are the clinical signs? |
1) Alkaloids called taxines.
2) Block Na mvmt & depress myocardium. 3) Collapse & sudden death, sometimes preceded by tremors & weakness. |
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Cardiac glycoside-containing plants 1) What is an example? 2) How do they work? 3) What do high doses result in? |
1) Digitalis purpurea (foxglove). 2) Digitalis-like action. Interfere with Na/K/ATPase leading to altered Na & K flux across membranes & increase in intracellular Ca; resulting in alterations of cardiac conduction. 3) Asystole & increased vagal tone to the SA node & AV node. |
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Oak (Acorn poisoning) 1) What parts are toxic? 2) What are the clinical signs? 3) What is the treatment? |
1) Oak blossom, leaves, stems, & acorns (livestock; horses mostly). 2) CS: colic, rectal tenesmus, hemorrhagic diarrhea, tachycardia, tachypnea, & presence of acorns in feces. May cause sudden death. 3) Tx: supportive therapy. |
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Selenium Toxicity 1) What causes this? 2) What presents with acute poisoning? 3) What presents with chronic poisoning? 4) How is it dx? 5) How is it tx? |
1) Ingestion of seleniferous plants or excessive admin of selenium supplements. 2) (Usually over supplementation). Acute CS: lethargy, weakness, colic, diarrhea, arrhythmias, & dyspnea. 3) Chronic CS: dramatic loss of mane & tail, thin fragile body hair. Lameness results from laminitis, hoof 'slippering' & sloughing. 4) Dx: based on hx & assays of selenium in mane/tail. 5) Tx: remove source of selenium & feed diets high in protein. |
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What is a major mycotoxin? Describe the condition. |
Aflatoxicosis. Usually produced by Aspergillus flavus & parasiticus. Form in CHOs in field & storage. Causes liver dz, colic, & can be fatal.
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Ryegrass Staggers 1) What causes growth promotion? 2) Why are certain weather conditions a concern? 3) What are the clinical signs? 4) How might they recover? |
1) Endophytes in certain grasses have symbiotic relationship w/grass. 2) Endophytes can produce neurotoxic alkaloids-staggers in grazing animals. 3) CS: Diffuse vestibulocerebellar syndrome w/hypometric ataxia, proprioceptive deficits, wide-based stance, m tremors, ataxic eyeball mvmts. Weakness NOT a feature. 4) Remove food source. |
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What is a zootoxin example? Describe the source & condition. |
Blister beetle toxicosis. Canthardidin intoxication from ingestion of dead beetles entrapped in hay at harvesting. Ingested canthardin causes infl & necrosis of GIT. Primarily causes severe colic in horses. Hypocalcemia. Can be fatal. |
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What is a main metal poisoning? |
Lead toxicity
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Lead Toxicity 1) What are potential sources? (3) 2) What are the clinical signs? (7) 3) How is it dx? 4) How is it tx? |
1) Lead-based paints, car batteries, and lead plumbing.
2) CS: weak, weight loss, dysphagia, proprioceptive deficits & m tremors, laryngeal paralysis (often bilateral). 3) Dx: blood or tissue lead concentrations. 4) Tx: eliminate source of lead. Chelation therapy (Ca disodium EDTA). |
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What is a concerning insecticide poisoning? |
Anticholinesterase insecticides
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Anticholinesterase insecticides 1) How do they work? 2) What are the clinical signs? 3) What may counteract parasympathetic signs? |
1) Carbamate pesticides depress acetylcholinesterase. 2) CS usually short-lived (36-48h)-recovery or death. CS (muscarinic or nicotinic overstimulation): profuse salivation, colic, lacrimation, miosis, sweating, dyspnea, coughing from excess respiratory secretions, & tetany of mm. Possible CNS depression or stimulation. 3) Atropine may counteract PS signs. |
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What is a big concern w/rodenticides/pesticides? How does it work? What does it cause? How is it treated? |
Warfarin toxicity. Competitively inhibits Vit K (used for clotting factors 2, 7, 9, & 10). Causes hemorrhagic diatheses. Tx w/vit K1.
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What is a therapeutic agent that may lead to toxicity in the horse? What does it cause? |
Vit K toxicity. Causes acute & chronic renal failure in horses.
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What is a feed additive concern for toxicity? |
Monensin toxicity |
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Monensin toxicity 1) What is monensin? 2) When is this routinely used? 4) What is the primary target? 5) What are the clinical signs? 8) What is CI? |
1) Polyether antibiotic (carboxylic ionophore). 2) Growth promoter in cattle. Coccidiostat in poultry. 3) Interferes w/transport of Na & K b/wn intracellular & extracellular spaces. 4) Heart. 5) CS vary: mild inappetance to sudden death from hypovolemic shock. Ataxia, m weakness, anorexia, colic, sweating, tachydysrhythmias, hemolysis, myoglobinuria, cardiac/renal/hepatic failure. 6) Dx: LV overload on echocardiography, bloods (elevated AST, CK), urinalysis. 7) Tx: supportive. 8) CI: Digitalis. |
